The TECHNOSCREEN ADAMTS-13 assay (ADSC) is a new lateral flow test which is simple and quick to perform, with a high negative predictive value (NPV); it may improve the diagnostic workflow for TTP. LabPlus in Auckland, New Zealand, performs all ADAMTS13 tests in the Auckland and Northland regions. The ADSC was used at LabPlus between 2022 and 2023 as part of a protocol where results of 0 IU/mL and 0.1 IU/mL were confirmed with the TECHNOZYM ADAMTS-13 Activity chromogenic ELISA assay (ADATS). The aim was to improve cost efficiency by reducing the need for the labour-intensive ADATS, particularly in low probability requests. This retrospective audit analyses the efficacy and efficiency of the testing protocol.
All ADAMTS-13 tests performed in the year before the ADSC (March 2021–March 2022) and after the ADSC protocol was introduced (March 2022–March 2023) were collected from the LabPlus laboratory information system (LIS), and correlated with clinical information from the electronic health record. Statistical analysis was performed.
Ninety-four test requests were audited. ADSC had an NPV of 100% on diagnostic samples. The protocol increased the median turn-around time (TAT) by 18 h (p = 0.01). If an ADSC of 0.1 IU/mL was taken as a negative, the median TAT was decreased by 17 h (p = 0.0003) in diagnostic samples from LabPlus adjacent hospitals.
ADSC has a high NPV but did not improve TAT when used as part of a testing protocol for our central laboratory receiving samples from a large area.
We aimed to identify additional predictors of severe fever with thrombocytopenia syndrome (SFTS), which has a significantly increasing global incidence.
This retrospective study included 95 patients with SFTS and 30 healthy individuals. Complete blood count with differential was performed using Sysmex XN 9000 and Mindray BC-6800 Plus analyzers. Extended leukocyte cell population data (CPD) parameters were acquired using a Mindray BC-6800 Plus analyzer. Peripheral smears were identified, and SFTS virus (SFTSV) RNA was detected using real-time reverse transcription polymerase chain reaction.
Of 95 patients with SFTS at admission, 75.8% (72/95) presented leukopenia and 96.8% (92/95) thrombocytopenia with SFTS. Neutrophil left shift and smudge cells (32.4/WBC ± 28.2/WBC) were observed 100% (57/57) on the blood smear. Only 21.1% (21/57) of the reactive lymphocytes were > 5% (3.24% ± 3.35%). Moreover, 33.3% (19/57) of apoptotic lymphocytes and 8.8% (5/57) of nucleated red blood cells were present. Furthermore, 78.9% (45/57) of reactive plasmacytoid lymphocytes increased 3–5 days after admission and 61.1% (11/18) of the patients who died presented with dust blue inclusions in the neutrophils. Compared to the control group, Neu-Y and all lymphocyte and monocyte CPD parameters were significantly higher in all SFTS groups. Compared to the surviving patients with SFTS, Lym-Y in Group 2 (p < 0.05) was significantly lower, but Neu-Y and Mon-Z in Group 3 were higher (p < 0.001) in the death group.
The cell count, peripheral blood morphology, and CPD parameters described in this study had a strong prompting effect on SFTSV infection.
The actual prevalence of the qualitative fibrinogen abnormalities dysfibrinogenemia and hypodysfibrinogenemia is unknown. The major reasons are that patients with dysfibrinogenemia are frequently asymptomatic, and a recommended screening test, the Clauss fibrinogen assay, cannot completely distinguish qualitative from quantitative abnormalities. We previously established a high-throughput screening test (Clauss-CWA) to identify dysfibrinogenemia with high specificity and sensitivity by the Clauss fibrinogen assay alone.
This was a single-center, observational study to estimate the prevalence of dysfibrinogenemia using Clauss-CWA technology. A total of 25 471 patients in Nagoya University Hospital were screened to identify patients with suspected dysfibrinogenemia. The suspected patients were investigated by further confirmatory analyses, such as antigenic fibrinogen determination, reptilase time, fibrin polymerization analysis, and scanning electron microscopy.
Of the 25 471 enrolled patients, five with suspected dysfibrinogenemia were identified. Unfortunately, one patient was not confirmed due to a lack of plasma samples. The ratio of functional to antigenic fibrinogen was decreased, and the reptilase time was prolonged in the four patients. Interestingly, two of them showed normal functional fibrinogen levels due to acute inflammatory responses. Fibrin polymerization was impaired, and structural abnormalities were found in the fibrinogen from the patients. In some cases, functional fibrinogen levels may not be effective for identifying functional fibrinogen abnormalities. Further nationwide studies are needed to more precisely understand the epidemiology of dysfibrinogenemia.
The recently published ACR/EULAR classification criteria score (3 points or more) both clinical and laboratory criteria to define the presence of antiphospholipid syndrome (APS). The clinical criteria have been better defined while laboratory criteria remain the same [lupus anticoagulant (LA), anticardiolipin (aCL) and anti ß2-Glycoprotein I (aß2GPI) antibodies] but with different impact (points) on the classification of patients. APS is excluded if more than 3 years separate positive test for antiphospholipid antibodies (aPL) and clinical manifestation.
The present study evaluates how many patients would be excluded by the new criteria among those enrolled as APS in the START 2 antiphospholipid registry. The analysis includes 380 patients (274 APS and 106 carriers).
Of 274 patients classified as APS, 118 (43%) did not match the new ACR/EULAR criteria for various reasons. First, the determination of aCL and aß2GPI antibodies was performed by automated instrumentations not allowed in the new criteria. Second, laboratory test score was less than 3 and this was due to an isolated IgM aCL or IgM aß2GPI in most cases and to isolated LA unconfirmed after 12 weeks in few cases. Third, 2 patients had a positive laboratory tests more than 3 years after the clinical event.
Of the 106 carriers, 62% had aCL and aß2GPI determined by ELISA thus meeting the ACL/EULAR laboratory criteria but were negative for clinical criteria.
This study shows that many patients classified as APS in the START 2 registry do not match the classification using the new ACR/EULAR criteria.
Hematology laboratories have traditionally monitored hemophilia replacement therapy by measuring coagulation factors before and after infusion. However, new drugs that do not rely on the replacement of the deficient factor require new approaches to laboratory monitoring, as factor VIII (FVIII) or factor IX (FIX) assays are no longer adequate. Non-factor therapies come in many different forms, that have one thing in common: they all increase thrombin generation. Their main adverse effect is thrombosis which may occur when too much thrombin is formed. This is the perfect mirror image of anticoagulant treatment, which always diminishes the amount of thrombin formed and has bleeding as its main adverse effect. Thrombin-forming capacity is decreased in congenital bleeding disorders and increased in prothrombotic conditions, indicating it governs bleeding and thrombosis. Therefore, the thrombin generation assay (TGA) is a logical tool for monitoring non-factor therapies, offering a comprehensive assessment of hemostatic balance. TGA identifies patients with severe bleeding, helps to optimize bypassing therapy, and detects hypercoagulability, making it ideal for guiding and monitoring hemophilia treatment with non-factor therapies. It also assesses the efficacy and safety of combined therapies, including non-factor therapies with bypassing agents or FVIII/FIX concentrates. The purpose of this paper is to review the current state of knowledge regarding the use of TGA to monitor novel hemophilia therapies. It will address controversies, limitations, and knowledge gaps related to the integration of TGA into personalized medicine in routine clinical practice.
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